Postpalatoplasty Fistulas: Diagnosis, Treatment, and Prevention


Postpalatoplasty Fistulas: Diagnosis, Treatment, and Prevention

Darren M. Smith, Matthew D. Ford, Joseph E. Losee


Palatal fistulas are extremely difficult to manage.

The best fistula management strategy is avoidance.

Tension-free, watertight primary palatoplasty must be achieved to prevent fistula formation.

Acellular dermal matrix may be used to ensure robust primary palatoplasty.

If a postoperative fistula develops, management options range from local flaps to free tissue transfer.

Postoperative fistulas are arguably the most significant concern for palatal surgeons, second only to the patient’s resultant quality of speech. Indeed, fistulas may themselves have deleterious effects on speech after palatoplasty as manifested by velopharyngeal insufficiency (VPI). Fistulas are most commonly ascribed to wound breakdown secondary to closure under tension, infection, flap trauma, hematoma, or compromise of the vascular pedicle resulting in tissue ischemia. Untreated fistulas may lead to nasal air escape, speech distortion, hearing loss, or regurgitation of fluid and food.1 These problems are compounded by the fact that fistulas are difficult to definitively repair. The incidence of cleft palate fistulas is reported to range from 0 to 76%, whereas the recurrence rate of palatal fistulas reportedly approaches 100%.25 The literature on this complication is confusing and difficult to interpret, partially because of vague definitions and a lack of standardized language addressing fistula location and clinical significance. Ambiguous literature has impeded progress in efforts to more effectively characterize and manage postpalatoplasty fistulas. Our approach to fistula classification, detailed here, is independent of etiology and functionality, and allows anatomic report on and consistent description of not only fistulas present after palatal repair, but also those with other causes, such as trauma and congenital deformities. In an effort to prospectively clarify the literature and advance the management of palatal fistulas, we introduced a standardized classification system for these lesions.6 This chapter discusses the proposed fistula classification system and examines palatal fistulas in terms of their cause, repair, and prevention.



Commenting on the confused state of the cleft palate literature, Emory et al7 contended, “Until a uniform definition of palatal fistula is utilized, it will be difficult to compare the results of different studies.” Some general definitions of palatal fistulas do exist; they have been described as an abnormal communication between two cavities, or as a complication of palatoplasty, occurring along the site of a palate repair.8,9 We find a definition that is both anatomically specific and independent of etiologic factors or functionality to be most useful: “A fistula is a patency between the oral and nasal cavities.” Literature dating from the 1950s to the present offers few suggested definitions for specific types of palatal fistulas.8,9 Folk et al8 described fistulas as occurring at the level of the soft palate, junction of the hard and soft palate, hard palate, incisive foramen, or anterior to the incisive foramen. In a report from the Children’s Hospital of Philadelphia, Cohen et al10 described fistulas as occurring at the level of the uvula, soft palate, hard palate-soft palate junction, hard palate, postalveolar, alveolar, and prealveolar regions. Despite these isolated accounts, establishing external consistency among studies in describing fistulas is extremely difficult, as no widely accepted and regularly used standardized classification system for palatal fistulas has evolved. For example, one author’s “alveolar fistula” might be another’s “lingual-alveolar fistula” and yet another’s “labial-alveolar fistula”; or one surgeon’s “hard palate fistula” may be another’s “incisive foramen fistula” and yet another’s “junction of the hard and soft palate fistula.”

Because clear nomenclature is a prerequisite to meaningful discussion, ongoing research, and evolving new treatment strategies, we developed a simple, logical, and anatomically based classification system to standardize fistula-related terminology.6 The resultant Pittsburgh fistula classification system includes seven fistula types (Fig. 57-1). Fistulas at the uvula, or bifid uvula, are considered type I fistulas (Fig. 57-2, A). Type II fistulas occur within the soft palate (Fig. 57-2, B). Type III fistulas are found at the junction of the soft and hard palates (Fig. 57-2, C). Type IV fistulas are located within the hard palate (Fig. 57-2, D).


Fig. 57-1 The Pittsburgh fistula classification system. Fistulas at the uvula, or bifid uvula, are type I fistulas. Soft palate fistulas are type II. Type III fistulas are at the junction of the soft and hard palates. Hard palate fistulas are type IV. Type V fistulas are at the incisive foramen, or junction of the primary and secondary palates. This designation applies only to fistulas in the context of Veau IV clefts. Type VI fistulas are lingual-alveolar, and type VII fistulas are labial-alveolar.


Fig. 57-2 Examples of fistulas according to the Pittsburgh fistula classification system. A, Type I: bifid uvula. B, Type II: soft palate. C, Type III: the junction of the hard and soft palates. D, Type IV: hard palate. E, Type V: the incisive foramen (junction of the primary and secondary palates); this designation reserved for Veau IV bilateral clefts. F, Type VI and VII fistulas: A, lingual-alveolar and, B, labial-alveolar.

Type V fistulas are defined as fistulas at the incisive foramen, or junction of the primary and secondary palates; this designation is reserved for use with Veau IV clefts (Fig. 57-2, E). Type VI fistulas are lingualalveolar, and type VII fistulas are labial-alveolar (Fig. 57-2, F).

We have found the Pittsburgh fistula classification system to be a functional, standardized scheme; clinical application in our cleft center has helped us to establish consistency in reporting and has thus facilitated clinical research. A numerical classification system seems critical for several reasons. Surgeons are notoriously inadequate in routinely reporting thorough anatomic descriptions of their outcomes, especially their complications. In a recent review, our group examined more than a majority of 640 charts spanning 25 years and representing 18 surgeons.6 This study revealed that in most cases, fistulas were frequently mentioned but inadequately described. In some cases, fistulas were noted by the speech pathologist and not addressed by the treating surgeon. When a fistula was documented, the description found in the medical record was commonly vague. Rarely did these notes address the location, size, or functionality of these fistulas. As our review revealed analogous ambiguity in the literature, a lack of internal and external consistency clearly renders intercenter, surgeon-specific, and procedure-related comparisons impossible. Therefore measures to standardize reporting, such as numerical systems, are paramount. In addition to defining a fistula in terms of its anatomic location, determining whether a fistula is functional or symptomatic as opposed to nonfunctional or asymptomatic is important. Simply put, if a fistula is clinically significant, it is said to be “functional” or “symptomatic.” Fistulas are clinically significant when they lead to nasal air escape, speech distortion, hearing loss, or regurgitation of fluid and food.1 Clinically significant fistulas may also induce VPI, which complicates speech management and outcome assessment.11 Finally, when discussing the incidence of postoperative fistulas, determining whether the fistulas in question were intentional (such as those resulting from deliberately unrepaired alveolar clefts) or unintentional (resulting from wound breakdown caused by closure under tension, infection, flap trauma, hematoma, or compromise of the vascular pedicle resulting in tissue ischemia). Functionality and intentionality may also be incorporated into the previously mentioned classification system. The addition of a prefix of (+) or (−) denotes functionality. Fistulas resulting in nasal air escape or nasal regurgitation of liquid or food (functional, symptomatic fistulas) would be reported with a (+), whereas nonfunctional, asymptomatic fistulas (not clinically significant) would be noted with a (−). Thus a (−) type V fistula would describe a nonfunctional or asymptomatic fistula at the junction of the primary and secondary palates in a Veau IV cleft. Analogously, a suffix may be added to indicate intentionality; for example, if a gingivoperiosteoplasty (GPP) was not performed, then type VI (lingual-alveolar) and type VII (labial-alveolar) fistulas would persist and the classification system would record them to be intentional.


Primary Fistulas or Palatal Clefts

Although the primary application of the Pittsburgh fistula classification system is for postoperative or secondary fistulas, it may be used to describe primary clefts as well. Primary fistulas are by definition congenital deformities; therefore palatal clefts can be classified as fistulas. Thus a Veau I cleft of the soft palate may accurately be described as Pittsburgh type I-II fistula, a Veau II cleft of the soft and hard palates is a Pittsburgh I-IV fistula, a Veau III unilateral complete cleft is a Pittsburgh I-IV/VI-VII fistula, and a Veau IV bilateral complete cleft is a Pittsburgh I-VII fistula.6

Secondary Fistulas

Secondary fistulas are either traumatic or iatrogenic (postoperative), and the reported rates of postoperative fistula formation range from 0 to 76%.24 As mentioned previously, postoperative fistulas can be described as intentional or unintentional. An intentional fistula exists after palatoplasty if the surgeon decides to leave a portion of the primary fistula (the cleft) patent. Intentional fistulas are most likely to arise in the context of a Veau III unilateral cleft or a Veau IV bilateral cleft in which the lingual-alveolar (Pittsburgh type VI) and labial-alveolar (Pittsburgh type VII) fistulas are left unrepaired—that is, in which a GPP is not performed. An unintentional fistula occurs as a complication after palatoplasty; the primary fistula, or cleft, is repaired, and a portion of the closure dehisces to produce a frank patency between the oropharynx and the nasopharynx. Although intentional fistulas are by definition the result of a conscious decision on the part of the operator, unintentional fistulas might have multiple causes. These causes can be conceptually divided into intrinsic causes and extrinsic causes. Intrinsic causes are those pertaining to qualities of the patient or lesions. For instance, Emory et al7 report that gender and the extent of clefting (as categorized by Veau classification) did not predict fistula formation rate. In contrast, Cohen et al10 found that fistulas were more common in patients with more severe clefts by Veau classification. Muzaffar et al1 saw a statistically significant increase in fistula formation for patients with Veau III and IV clefts over those with Veau I and II clefts. Schultz12 reported a positive correlation between both cleft type and width of the cleft and postoperative fistula formation. Cohen et al10 found that age at repair did not influence the rate of fistula formation. In contrast, Emory et al7 reported that patients undergoing palatal repair younger than 12 months of age had a lower incidence of fistula formation than those undergoing repair between 12 and 25 months of age (7.8% versus 19.4%, p <0.058). However, as reemphasized by Honnebier et al,14 the younger patients in this series were treated by more experienced palatal surgeons. Moore’s group15 found no association between age, sex, associated syndrome, history of otitis media, weight, preoperative hematocrit, tympanostomy tube placement, or cleft type and fistula formation. Sex and age were not found to be predictive of fistula formation by Muzaffar’s group.1 Schultz12 also found age to be insignificant in this context.

Extrinsic causes are those more related to surgical technique and operative strategy than to patient-specific qualities. Some of the most commonly cited extrinsic causes of these lesions are tension, absent multilayer repair, and poor surgical technique.5,16 Cohen et al10 found that the individual surgeon influences fistula rate. In fact, Emory et al7 assert that the surgeon performing the repair was the strongest predictor of fistula formation in their experience. In contrast, Muzaffar et al1 saw no association between surgeon and fistula rate. Interestingly, in their 1979 report on 845 palatoplasty patients, Abyholm et al16 note that the rate of fistula formation was less for those patients undergoing palatal repair between 1962 and 1969 than those having the surgery between 1954 and 1961. This group theorizes that progress in knowledge, surgical technique, and anesthesia are responsible for the observed improvement in surgical outcome. Moore’s group15 noticed a similar decline in fistula rates over time and reported no fistulas during the last 7 years of their 21-year series. Reports examining an association between surgical technique and perioperative procedures and fistula formation are disparate. Cohen et al10 reports palatoplasty technique to influence fistula rate; specifically, fistula occurrence rates were 43%, 22%, 10%, and 0% for patients undergoing Wardill-Kilner, von Langenbeck, Furlow, and Dorrance repairs, respectively. Moore et al15 corroborate the assertion that the Wardill-Kilner repair is most prone to postoperative fistula formation and attribute this finding to the convergence of three suture lines at one point as a result of this procedure. In contrast to these reports, Schultz,12 Emory et al,7 and Muzaffar et al1 found that surgical technique did not influence fistula rate. Intravelar veloplasty did not affect the rate of fistula formation in the Cohen or Moore series.10,15 Moore et al15 further report that intrapalatal epinephrine injection and intraoperative blood products did not affect fistula rate. In a recent review of 310 consecutive patients, we saw no relationship between perioperative antibiotic administration and the rate of fistula formation.17 Preoperative orthodontics are not associated with fistulas: Muzaffar et al1 found that palatal expansion and presurgical orthopedics did not predispose to fistula formation. Postoperative palatal manipulation, however, may cause fistula formation: Bardach and colleagues2,18 and Schultz12 cite maxillary expansion and segment movement, respectively, as having an association with palatal fistulas.

Tertiary Fistulas

Tertiary palatal fistulas result from the breakdown of the attempted repair of a postoperative fistula. Fistulas are extremely recalcitrant lesions, with recurrence rates reported to approach 100%.5 This susceptibility to recurrence is not surprising given the mucosal scarring from primary palatoplasty, poor vascularization, and the lack of compliance of local tissues.19 Rintala20 notes the paradoxical difficulty inherent in repairing smaller fistulas: the size of these lesions hinders the complete removal of the epithelial tract between the oral and nasal cavity. Analyses of factors predisposing to tertiary fistula formation are not robust. Multivariate statistical analysis performed by Cohen et al10 was able to validate only gender as predictive of fistula recurrence. This group found that cleft type, cleft repair technique, and site of the postoperative fistula were not predictive in this regard; small sample size precluded an analysis of fistula closure technique in this context. Similarly, Rintala20 was unable to comment on the relative efficacy of fistula repair techniques. In addition to breakdown and tertiary fistula formation, fistula repairs themselves can be morbid, leading to tissue loss at the donor site, hindrance of maxillary growth from scar contracture, and poor aesthetic outcomes.14


It is not surprising that this recalcitrant lesion has inspired treatment strategies spanning the reconstructive ladder. One of the most direct approaches to fistula management, chemical cauterization, was described by Obermeyer21 in 1967. Berkman22 designed a continuously worn vinyl appliance to guide local healing of fistulas recognized early and addressed immediately with steadfast patient compliance upon discovery.

Local flap options for fistula repair are numerous; the origins of these procedures are reviewed by Millard,23 from von Langenbeck’s 1864 turnover hinge flap to Gabka’s 1964 V-Y advancement flaps. Figs. 57-3 through 57-7 offer historical examples. Guerrero-Santos and colleagues24,25 popularized the tongue flap in the 1960s and 1970s. Ohsumi et al26 used free conchal cartilage grafts in this context. Recent reviews describe the application of free flaps with microvascular anastomoses in fistula closure.2730 Despite the wealth of creativity that has been invested in approaches to the postpalatoplasty fistula, the recurrence rate of this refractory lesion has been reported to approach 100%.5


Fig. 57-3 In 1964, Gabka illustrated a rotation flap for closure of a hard palate (type IV) fistula.


Fig. 57-4 Gabka demonstrated simultaneous closure of an alveolar (type VI-VII) fistula and a hard palate (type IV) fistula with a V-Y mucoperiosteal flap.


Fig. 57-5 Guerrero-Santos described this distally based dorsal tongue flap in 1966.


Fig. 57-6 Closure of a soft palate (type II) fistula with lateral relaxing incisions for mobilization of the hard palate mucoperiosteum, as described by O’Neal in 1971. The fistula edges are turned in, and three-layer closure is achieved.


Fig. 57-7 The waltzing unilateral dorsal tongue flap described by Guerrero-Santos in 1973.


Nonsurgical Options

The mainstay of nonsurgical treatment is the palatal obturator. Because of local irritation and discomfort related to the bulk of the appliance, patient compliance is poor.5 Moreover, because these devices are “high maintenance,” requiring frequent adjustment and meticulous hygienic attention, their use should be restricted to cases in which surgery is contraindicated.5 In a variation on the prosthetic obturator, Berkman22 reports that, with maximal patient compliance and identification of fistulas shortly after their appearance, a vinyl palatal appliance can be used to promote closure of these lesions by granulation, epithelialization, and fibrosis. This approach, however, seems fraught with the same limitations discussed for the standard palatal obturator. Furthermore, as Rintala20 notes, the potential of these repairs to withstand maxillary expansion is questionable.

Surgical Options

The surgical management of palatal fistulas can be a technically frustrating task. The surgical method chosen will depend on the fistula’s location and size, the status of nearby palatal tissues, availability of flap donor sites, type of original cleft, previous methods of repair, and surgeon preference. Every effort should be made to adhere to the following surgical principles in treating fistulas:

  1. Complete separation of the oral and nasal lining from one another, or judicious excision of the epithelialized tract
  2. Wide dissection of the nasal lining and mucosal flaps
  3. A tension-free, watertight, layered closure of the nasal lining and oral mucosa
  4. Perfect coaptation of wound edges
  5. Avoidance of overlapping suture lines
  6. Use of acellular dermal matrix as a third layer of soft tissue closure, placed between the nasal lining and oral mucosal repair
  7. Use of imported, well-vascularized tissue (such as a facial artery musculomucosal [FAMM] flap) if complete oral mucosal repair is not possible with well-vascularized local palatal tissue
  8. Strict postoperative care

No single surgical procedure will fulfill all these criteria in treating palatal fistulas. The palate is usually heavily scarred with little to no extensibility. Moreover, larger fistulas require more tissue for closure, and less local tissue is available in the setting of a large defect. This surgical difficulty has incited surgeons to use a myriad of local, regional, and distant flaps, grafts, and alloplastic material to improve their results.

Simple Closure

Simple closure is probably the most common procedure used and can adequately treat a large proportion of fistulas. This basic technique, essentially a recapitulation of the primary closure, consists of an incision at the margins of the fistula to create medial turnover flaps or “hinge flaps” for nasal lining closure (Fig. 57-8). These medial flaps are extended anteriorly and posteriorly along the midline palatal scar.

For wide fistulas, the marginal incision around the defect may be made several millimeters away from the edge of the defect to facilitate the harvest of tissue and allow a nasal lining repair. In addition, if the fistula is within the hard palate, vomer flaps may also be used to obtain a nasal lining closure. Lateral relaxing incisions are made at the junction of the attached gingiva and hard palate tissue and are used to elevate palatal mucoperiosteal flaps. Alternatively, these relaxing incisions can be placed at the apex of the gingiva, removing the attached gingiva from the teeth and including it in the palatal flaps, adding a small but significant amount of length to the palatal flaps. The reported complication of gingival recession with this approach is rare in the young population.31


Fig. 57-8 A type IV (hard palate) fistula with outline of the medial paring incision and the lateral releasing incisions.

The palate is often heavily scarred and unyielding after primary palatoplasty, and the entire palate often has to be elevated with bipedicled or unipedicled flaps and mobilization of the greater palatine vessels. Underestimating the degree of palatal mobilization required is a common mistake; even in small fistulas the palatal mucoperiosteum should be widely freed to avoid tension on the closure line. In addition, wide dissection allows complete excision of the mucosalized granulation tissue at the fistula site and proper undermining and closure of the nasal layer. Some authors argue that closure of the nasal layer is not essential and that many patients can have permanent ablation of the fistula by a single-layer closure alone; however, because recurrence rates are high, closing both layers is advantageous, especially because careful technique makes dual-layer closure practical.32 In fact, as mentioned in many of the techniques discussed in the following sections, a triple-layer repair is sometimes advocated. Our preferred technique is to add a third layer of acellular dermal matrix, sandwiched between the nasal and oral linings, even if an adequate repair of both layers is obtained. After obtaining a nasal lining repair, transposing the palatal flaps laterally off to one side of the nasal suture line and avoiding overlapping of the suture lines is preferable.

A helpful technique is to start the entire procedure with the lateral relaxing incisions, elevating the oral mucoperiosteum and identifying and dissecting the fistula tract (from superficial to deep) before transecting the fistula. This sequence will allow accurate placement of the medial incision and separation of the oral and nasal linings.


Palatal Flaps Various palatal flaps have been described in the literature to treat palatal fistulas. Hinge flaps or turnover flaps are palatal mucosal flaps from the immediate vicinity of the fistula that are based on the fistula mucosa. These flaps are hinged on their base and turned over to provide nasal layer closure.33 Although they involve a simple procedure with minimal donor site morbidity, hinge flaps have definite limitations: These flaps can only be used to provide nasal closure for small fistulas, are based on the original scar with questionable vascularity, and prevent complete excision of the scarred tissue in the fistula tract.

Other local flaps from the palate can be raised in a random fashion and used as transposition or rotation flaps for oral layer closure (Fig. 57-9). Despite the arc of rotation and transposition noted in illustrations, in reality these flaps are very limited in size and excursion. A variant of these flaps is the hemi-palatal island flap, in which almost an entire half of the hard palate mucosa is raised based on the greater palatine vessels.34 After visualizing the vessels on the undersurface of the flap, a transverse cut is made in the palatal mucosa behind the vessels to completely free the flap and allow its transposition across the midline. Although this procedure will provide ample tissue for oral closure without overlapping suture lines, it involves a radical dissection, relies on integrity of the greater palatine vessels after the primary repair, and leaves significant raw areas for spontaneous healing.35

Regional Flaps The paucity of tissue in a scarred palate has led surgeons to design flaps using the mucosa of the cheek, tongue, and gingiva. Random flaps from the cheek or vestibular mucosa are limited in size and reach. Axial pattern flaps, however, are more difficult to design and elevate. In addition, axial pattern flaps have a tenuous course to the midline of the palate. The most common regional flaps described for the treatment of palatal fistulas include gingival flaps, the buccinator myomucosal flap, the FAMM flap, and tongue flaps. Although they can be used for closure of the nasal layer or as an interposition between the oral and nasal closures, these flaps are most commonly used for closure of the oral mucosa. This strategy allows more oral palatal tissues to be recruited for a secure nasal layer closure, even in large fistulas.

Vestibular Mucosal Flaps The gingival (vestibular) mucosal flaps, raised from the labial side of the alveolus, are one of the most commonly used flaps for both alveolar bone grafting and anterior palatal fistula closure.36 Although they are random flaps, gingival mucosal flaps have a reliable vascular supply. These flaps are usually raised with their width equal to the height of the alveolus and extend along the alveolar ridge (Fig. 57-10); they are transposed to the anterior palate through the alveolar defect. This technique may interfere with growth of the maxilla and future orthodontic expansion and surgery (for example, bone grafting of the alveolar cleft). Alternatively, they can be passed through a subperiosteal tunnel at the floor of the nose to the nasal side of the fistula; however, this is a lengthy dissection and a tight tunnel. Other designs have been used, such as leaving an exteriorized pedicle for later separation, raising bilaterally based bucket handle flaps, or elevating an island flap.37,38 If an excessive amount of mucosa is harvested, distortion of the shape of the lip may result, or at best the mucosa will be unavailable in future surgeries.37


Fig. 57-11 A, Design of the buccal mucosal flap. B, The flap turned over to close the nasal layer. C, After closure of the oral layer over the flap.

Buccal Mucosal Flaps Buccal flaps have been described to augment nasal layer closure both in primary clefts and in palatal fistulas.39 They are especially helpful in type III fistulas (at the junction of the hard and soft palates), which are infamous for their paucity of local tissue; moreover, these flaps may augment palatal length. They are raised from the cheek with their base behind the upper alveolus with a width of 1.5 to 2 cm (Fig. 57-11). Buccal mucosal flaps are random flaps containing mucosa and submucosal tissue. When raising the flap, the surgeon must avoid the parotid duct (although this is rarely problematic) and prevent exposure of the buccal fat pad (BFP). The flap is turned over, passed in a submucosal tunnel behind the edge of the hard palate, and sutured to the edges of the nasal mucosa. The donor site is closed primarily. Alternatively, the flap can be used to close the oral layer, usually leaving an exteriorized pedicle to be separated in 2 to 3 weeks.

Buccinator Myomucosal Flap The buccinator muscle has a rich arterial, venous, and nerve supply, allowing elevation of flaps that are reliable, sensate, and of variable dimensions while preserving the function of the remaining muscle.40 The buccal artery (a branch of the internal maxillary artery) and the posterior buccal branches of the facial artery are the basis of the posteriorly based buccinator myomucosal flap.41,42 Both arteries enter the posterior portion of the muscle, and their diameters are inversely proportional. The upper border of the flap extends from the posterior aspect of the maxilla to the oral commissure and is 3 to 10 mm below the parotid duct orifice. Alternatively, the anterior limit of the flap can extend further into the lips, creating a Y-shaped flap.42 The flap’s width is approximately 1 to 3 cm, thus allowing primary donor site closure. The mucosa and muscle are incised to create either a peninsular or island flap. The muscle is elevated and separated from the deep buccopharyngeal fascia in a loose areolar plane. Dissection in this plane should proceed rapidly and easily, preserving the integrity of the fascia and thus preventing prolapse of the BFP or injury to the facial nerve.41 The flap’s length can approach 10 cm, running posteriorly to the level of the pterygomandibular raphe.

Facial Artery Musculomucosal Flap Like the buccinator myomucosal flap, the FAMM flap is raised from the cheek mucosa and includes a portion of the buccinator muscle. Although it has been argued that this flap is only a variant of the buccinator flap, it is a distinct entity in its inclusion of the facial artery.43,44 The flap is designed along the course of the facial artery, which can be palpated or mapped by a Doppler probe (Fig. 57-12). The flap has an oblique orientation, from the retromolar trigone to the gingivolabial sulcus at the base of the ipsilateral alar crease, with a width of 1.5 to 2 cm and a length up to 9 to 11 cm.45 The flap is designed anterior to the orifice of the parotid duct. It is elevated to include the mucosa, part of the buccinator and orbicularis oris, and the facial artery.

The venous drainage is either through the facial vein or through the random but robust venous plexuses around the facial artery. The flap can be based superiorly, to reach alveolar and hard palate fistulas (types IV through VII), or inferiorly and posteriorly to reach soft palate fistulas (types I through III). After the margins of the flap are incised, the facial artery is ligated at the distal end of the flap and dissection proceeds to include the mucosa, part of the buccinator and orbicularis oris, and the facial artery. The donor site is closed in two layers (muscle and mucosa). The flap usually requires an open dental arch for passage to the palate (for example, through an alveolar cleft). Inferiorly based flaps can be used in a two-stage fashion, with the flap turning behind and around the maxillary tuberosity with an exteriorized pedicle for later division and insetting. This will necessitate the use of a bite block secured to the dentition for 2 weeks to prevent trauma to the flap. Other drawbacks include the bulk of the flap (which can be secondarily corrected if necessary) and initial tightness at the donor site (which usually resolves spontaneously). Some speech therapists have discouraged the use of this flap because of possible interference with facial muscles and speech development; however, this has not been shown to be a long-term problem. The FAMM flap is fairly reliable and provides enough mucosa to cover large fistulas or create a double layer closure.45


Fig. 57-12 A, Design of a superiorly based FAMM flap showing its reach to the hard palate, lip, or nose. B, Design of an inferiorly based FAMM flap reaching the floor of the mouth (1), soft palate (2), or hard palate (3).

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May 11, 2019 | Posted by in Oral and Maxillofacial Surgery | Comments Off on Postpalatoplasty Fistulas: Diagnosis, Treatment, and Prevention
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